Zika virus disrupts molecular fingerprinting of human neurospheres

Garcez, Patrícia P.; Nascimento, Juliana; Vasconcelos, Janaína Mota de; Costa, Rodrigo Madeiro da; Delvecchio, Rodrigo; Trindade, Pablo; Loiola, Erick Correia; Higa, Luiza M.; Cassoli, Juliana S.; Vitória, Gabriela; Sequeira, Patrícia Carvalho de; Sochacki, Jaroslaw; Aguiar, Renato Santana; Fuzii, Hellen Thaís; Filippis, Ana María Bispo de; Júnior, João Lídio da Silva Gonçalves Vianez; Tanuri, Amílcar; Martins-de-Souza, Daniel; Rehen, Stevens K.

doi:10.1038/srep40780

Cited by 107 publications

(100 citation statements)

References 61 publications

(81 reference statements)

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“…On the following day, media was changed to remove iROCK. Neurons were cultured until day [30][31][32][33][34][35] to perform experiments and viral infection.…”

Section: Discussionmentioning

confidence: 99%

Zika virus infection leads to mitochondrial failure, oxidative stress and DNA damage in human iPSC-derived astrocytes

Ledur

Karmirian

Pedrosa

et al. 2020

Sci Rep

Self Cite

102

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Zika virus (ZiKV) has been extensively studied since it was linked to congenital malformations, and recent research has revealed that astrocytes are targets of ZiKV. However, the consequences of ZiKV infection, especially to this cell type, remain largely unknown, particularly considering integrative studies aiming to understand the crosstalk among key cellular mechanisms and fates involved in the neurotoxicity of the virus. Here, the consequences of ZiKV infection in ipSc-derived astrocytes are presented. our results show RoS imbalance, mitochondrial defects and DnA breakage, which have been previously linked to neurological disorders. We have also detected glial reactivity, also present in mice and in post-mortem brains from infected neonates from the northeast of Brazil. Given the role of glia in the developing brain, these findings may help to explain the observed effects in congenital Zika syndrome related to neuronal loss and motor deficit.

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“…On the following day, media was changed to remove iROCK. Neurons were cultured until day [30][31][32][33][34][35] to perform experiments and viral infection.…”

Section: Discussionmentioning

confidence: 99%

Zika virus infection leads to mitochondrial failure, oxidative stress and DNA damage in human iPSC-derived astrocytes

Ledur

Karmirian

Pedrosa

et al. 2020

Sci Rep

Self Cite

102

111

View full text Add to dashboard Cite

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“…DENV can raise the level of tumour necrosis factor α (TNF‐α) and expression of 151 genes, such as those encoding CD14, CD274, h2‐ea, Tap1, Tap2, and Stat2 . Over 500 proteins and genes were differentially expressed with ZIKV infection …”

Section: Possible Mechanisms Underlying Flavivirus‐induced Neuronal Lmentioning

confidence: 99%

“…We propose possible mechanisms of intracellular effects that lead to ZIKV neurotoxicity. According to activation of the JAK‐STAT pathway, the STAT2 gene will be upregulated and the STAT1/STAT2 pathway will be activated. We speculate that the JAK‐STAT signalling pathway plays a role in the effects observed in ZIKV‐infected neurons.…”

Section: Hypothesis For Zikv‐induced Neurotoxicitymentioning

confidence: 99%

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Research advancements in the neurological presentation of flaviviruses

Chen

Zhang

et al. 2018

Reviews in Medical Virology

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Summary Owing to the large‐scale epidemic of Zika virus disease and its association with microcephaly, properties that allow flaviviruses to cause nervous system diseases are an important area of investigation. At present, although potential pathogenic mechanisms of flaviviruses in the nervous system have been examined, they have not been completely elucidated. In this paper, we review the possible mechanisms of blood‐brain barrier penetration, the pathological effects on neurons, and the association between virus mutations and neurotoxicity. A hypothesis on neurotoxicity caused by the Zika virus is presented. Clarifying the mechanisms of virulence of flaviviruses will be helpful in finding better antiviral drugs and optimizing the treatment of symptoms.

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“…Studies using an Asian strain of ZIKV (FSS13025, isolated in Cambodia) or ZIKV isolated from recent outbreaks in Brazil (Cugola et al, 2016;Souza et al, 2016;Garcez et al, 2017;Sacramento et al, 2017), Puerto Rico (Hanners et al, 2016;Wells et al, 2016) and French Polynesia (Ghouzzi et al, 2016) have shown the ability of the virus to infect and induce apoptosis of human NPC.…”

Section: Zikv Induces Apoptosis Autophagy and Mitotic Abnormalities mentioning

confidence: 99%

Zika Virus: What Have We Learnt Since the Start of the Recent Epidemic?

2018

Frontiers Research Topics

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Zika is a viral disease transmitted mainly by mosquitoes of the genus Aedes. In recent years, it has expanded geographically, changing from an endemic mosquito-borne disease across equatorial Asia and Africa, to an epidemic disease causing large outbreaks in several areas of the world. With the recent Zika virus (ZIKV) outbreaks in the Americas, the disease has become a focus of attention of public health agencies and of the international research community, especially due to an association with neurological disorders in adults and to the severe neurological and ophthalmological abnormalities found in fetuses and newborns of mothers exposed to ZIKV during pregnancy. A large number of studies have been published in the last 3 years, revealing the structure of the virus, how it is transmitted and how it affects human cells. Many different animal models have been developed, which recapitulate several features of ZIKV disease and its neurological consequences. Moreover, several vaccine candidates are now in active preclinical development, and three of them have already entered phase I clinical trials. Likewise, many different compounds targeting viral and cellular components are being tested in in vitro and in experimental animal models. This review aims to discuss the current state of this rapidly growing literature from a multidisciplinary perspective, as well as to present an overview of the public health response to Zika and of the perspectives for the prevention and treatment of this disease.

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Zika virus disrupts molecular fingerprinting of human neurospheres

Cited by 107 publications

References 61 publications

Zika virus infection leads to mitochondrial failure, oxidative stress and DNA damage in human iPSC-derived astrocytes

Zika virus infection leads to mitochondrial failure, oxidative stress and DNA damage in human iPSC-derived astrocytes

Research advancements in the neurological presentation of flaviviruses

Zika Virus: What Have We Learnt Since the Start of the Recent Epidemic?

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